The studies will examine the pathological changes in bladder and pelvic ganglia of the cat and rat following sacral lower motor neuron (SLMN) lesions. The symptoms appearing in these species following SLMN lesions resemble those seen in humans who have sustained similar lesions. A frequent immediate clinical consequences of SLMN lesions is bladder areflexia and urinary retention. Over a period of weeks or months, some bladder activity may appear. This activity results in partial bladder emptying if urethral sphincter innervation is not damaged, or incontinence if the sphincter pathways have been interrupted. Gradually, bladder tone tends to increase abnormally. The mechanisms responsible for the hypertonic autonomous bladder are far from clear and the treatment of the symptoms remains problematical. These studies combine a) intracellular recording, b) dye injection and c) immunohistochemistry to examine the resulting pathophysiology. It seems likely that reinnervation from sympathetic, preganglionic fibers or even from ganglion cells within the same or adjacent ganglia (axonal sprouting) plays a prominent role in the development of bladder hypertonicity. Changes in transmitter mechanisms such as the development of non-cholinergic excitatory responses and the emergence of hypersensitivity to at least one peptide transmitter (SP) develop with a time course that parallels the appearance of the hypertonic condition. The unmasking of local reflexes (afferent to efferent connections) which seem nonexistant in acutely lesioned ganglia may be responsible for the appearanc of apparently "spontaneous" ganglionic cell firing in chronically lesioned preparations, and may contribute to the pathology. Lesions of the sacral ventral roots (removing the sacral preganglionic input) or pelvic nerve resection (interruption of both afferent and efferent sacral pathways) alone or in combination with resection of the hypogastric nerve will establish the relative contributions of 1) neural reorganization, 2) changes in transmitter mechanisms, and 3) unmasking of local reflexes, to the reappearance of bladder activity following nerve injury. It is anticipated that the results of these studies will have general application to questions of nerve injury and reinnervation and to neurogenic autonomic dysfunction of different etiology and different organ systems.